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Microrna‑148A‑3P Inhibits the Proliferation of Cervical Cancer Cells by Regulating the Expression Levels of DNMT1 and UTF1

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Microrna‑148A‑3P Inhibits the Proliferation of Cervical Cancer Cells by Regulating the Expression Levels of DNMT1 and UTF1 ONCOLOGY LETTERS 22: 617, 2021 MicroRNA‑148a‑3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1 QING CHEN1, YIDONG WANG1, HUIMIN DANG2 and XIAOLING WU1 Departments of 1Obstetrics and Gynecology, and 2Integrated Traditional Chinese and Western Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China Received January 31, 2021; Accepted May 21, 2021 DOI: 10.3892/ol.2021.12878 Abstract. MicroRNAs (miRs) serve a key role in carcinogen‑ of these cases occured in developing countries (3). Currently, esis. miR‑148a‑3p has been demonstrated to act as a tumor recurrence, metastasis and drug resistance are the major suppressor in several tumors, such as epithelial ovarian cancer obstacles encountered in the treatment of cervical cancer (4). and esophageal cancer. However, to the best of our knowledge, Therefore, the pathogenesis of cervical cancer requires further the role of miR‑148a‑3p in cervical cancer remains unclear. investigations to improve current treatment options. In the present study, the expression levels of miR‑148a‑3p MicroRNAs (miRNAs/miRs) have been demonstrated measured by reverse transcription‑quantitative PCR were to serve an important role in tumorigenesis (5,6). miRNAs significantly decreased in cervical cancer tissues compared are a group of small, non‑coding RNAs ~22 nucleotides with that in normal cervical tissues. Furthermore, overexpres‑ in length (7). miRNAs function as guide molecules in gene sion of miR‑148a‑3p markedly suppressed the proliferation of silencing and translational repression by binding to the cervical cancer cells. The luciferase reporter assay demon‑ 3'‑untranslated region (3'‑UTR) of their target mRNAs (8). strated that DNA methyltransferase 1 (DNMT1) was the Abnormal expression of miRNAs is closely associated with target gene of miR‑148a‑3p and that its expression measured tumor initiation, progression and prognosis (9). miR‑148a is by western blotting was inhibited by miR‑148a‑3p in cervical a novel tumor suppressor gene, which is involved in various cancer cells. Correlation analysis highlighted that the expres‑ biological functions, including cell apoptosis, cell cycle arrest sion levels of the undifferentiated embryonic cell transcription and cell senescence (10,11). The expression levels of miR‑148a factor‑1 (UTF1) were negatively associated with the expres‑ have been reported to be dysregulated in various cancer types, sion levels of DNMT1 in cervical cancer tissues. Furthermore, such as prostate, pancreatic (12) and colorectal cancer (13). DNMT1 knockdown increased the expression of UTF1 and However, to the best of our knowledge, the effects and under‑ decreased the methylation level of UTF1 promoter. These data lying molecular mechanism of miR‑148a‑3p in cervical cancer demonstrated the expression levels of UTF1 were regulated by remain unclear. Therefore, the present study aimed to investi‑ DNMT1 methylation in cervical cancer cells. Collectively, the gate the effects and the mechanism of miR‑148a‑3p in cervical results of the present study suggested that miR‑148a‑3p may cancer. The findings provide potential therapeutic targets for inhibit the proliferation of cervical cancer cells by regulating cervical cancer. the expression levels of DNMT1/UTF1, which provides poten‑ tial therapeutic targets for cervical cancer. Materials and methods Introduction Patient tissue samples. A total of 20 cervical cancer (mean ± SD age, 56±10.05 years; age range, 39‑68 years old, Cervical cancer is one of the most common malignant tumors all female) and 8 normal cervical samples (mean ± SD age, to occur in women (1). An estimated 527,600 new cases of 53±9.13 years; age range, 40‑65 years old, all female) were cervical cancer were diagnosed worldwide and 265,700 collected from patients that underwent surgical resection at The women succumbed to this disease in 2012 (2). The majority Second Affiliated Hospital of Xi'an Jiaotong University (Xi'an, China) between February 2017 and February 2018. In cases with histologically confirmed cervical cancer, only patients who underwent diagnostic procedures, such as biopsy were Correspondence to: Dr Xiaoling Wu, Department of Obstetrics included. Any patients with non‑epithelial cervical cancer, and Gynecology, The Second Affiliated Hospital of Xi'an Jiaotong recurrent disease and other malignancies were excluded from University, 157 Xiwu Road, Xi'an, Shaanxi 710004, P.R. China the present study. The normal cervical tissues were obtained E‑mail: [email protected] from patients with uterine leiomyoma. None of the patients had received chemotherapy, immunotherapy or radiotherapy Key words: DNA methyltransferase 1, microRNA‑148a‑3p, cervical prior to specimen collection. All tissue samples were frozen in cancer, methylation, cell proliferation liquid nitrogen at ‑80˚C until required for further experiments. The present study was approved by the Ethics Committee of 2 CHEN et al: miR‑148a INHIBITS CERVICAL CANCER CELL PROLIFERATION The Second Affiliated Hospital of Xi'an Jiaotong University Cell transfection. miR‑148a‑3p mimic (5'‑UCA GUG CAC (Xi'an, China) and the patients provided written informed UAC AGA ACU UUG U‑3'), miRNA mimic control (5'‑TTC consent prior to sample collection. TCC GAA CGT GTC ACG T‑3'), DNMT1‑short hairpin (sh) RNA plasmid expression vector (pGPU6/GFP/Neo, 5'‑GGAU Cell lines and culture. The HeLa and SiHa human cervical GAG UCC AUC AAG GAA TT‑3') and control‑shRNA (5'‑UUC cancer cell lines and human embryonic kidney cell line 293T UCC GAA CGU GUC ACG UTT‑3') were purchased from were purchased from American Type Culture Collection and Shanghai GenePharma Co., Ltd. Cells were incubated (1x105) cultured in DMEM (Sigma‑Aldrich; Merck KGaA) supple‑ in a 6‑well plate for at 37˚C for 24 h before transfection and mented with 10% heat‑inactivated FBS (Invitrogen; Thermo transfected with either miR‑148a‑3p mimic, control mimic, Fisher Scientific, Inc.), 80 U/ml penicillin and 80 ug/ml strep‑ DNMT1‑shRNA and control‑shRNA at a final concentration ® tomycin. The cells were maintained at 37˚C with 5% CO2. of 50 nM using Lipofectamine 2000 transfection reagent (Invitrogen; Thermo Fisher Scientific, Inc.) at 37˚C for 5 h Reverse transcription‑quantitative PCR (RT‑qPCR). Total according to the manufacturer's protocol. After 48 h, the cells RNA was extracted from frozen samples and cell lines using were used for subsequent experiments. TRIzol® reagent (Invitrogen; Thermo Fisher Scientific, Inc.). RT reactions were performed using the PrimeScript Luciferase reporter assay. 293T cells were seeded into a RT reagent kit (Takara Bio, Inc.) according to the manu‑ 24 well plate at a density of 5x104 cells/well. Following incuba‑ facturer's protocol. Subsequently, qPCR was performed tion at 37˚C for 24 h, a wild type or mutated DNMT1 3'‑UTR using the SYBR‑Green Master mix (Takara Bio, Inc.) luciferase reporter vector (Promega Corporation), combined according to the manufacturer's protocol. GAPDH and U6 with miR‑148a‑3p mimics (5'‑UCA GUG CAC UAC AGA spliceosomal RNA were used as an internal control for the ACU UUG U‑3'; Shanghai GenePharma Co., Ltd.) or miRNA quantification of mRNAs and miRNAs, respectively. The mimic control (5'‑TTC TCC GAA CGT GTC ACG T‑3', Shanghai primer sequences are shown in Table I. The thermocycling GenePharma Co., Ltd.), were transfected into the cells at a conditions were as follows: Pre‑denaturation at 50˚C for final concentration of 20 nM using a Vigofect transfection 2 min, denaturation at 95˚C for 10 min, annealing at 95˚C reagent [Weiglas Biotechnology (Beijing) Co., Ltd.] according for 30 sec and extension at 60˚C for 30 sec (40 cycles). The to the manufacturer's protocol. At 48 h post‑transfection, relative gene expression was quantified using the 2‑ΔΔCq the firefly and Renilla luciferase activities were detected method (14). using the Dual‑Luciferase Reporter assay system (Promega Corporation). Renilla luciferase activity was used as the Cell Counting Kit‑8 (CCK‑8) assay. Cell proliferation internal control. was measured using a CCK‑8 assay (Beyotime Institute of Biotechnology). Briefly, 1x103 cells/well were cultured in Bisulfite sequencing. Bisulfite sequencing was carried out 96‑well plates and assessed the following day. The assessment as previously described (15). Genomic DNA was extracted was carried out for 6 days in total. At the same time point on from SiHa and HeLa cells using the Universal Genomic DNA 2, 4, 6 days, 10 µl CCK‑8 solution was added to each well and Extraction kit (cat. no. DV811A; Takara Bio, Inc.) according the samples were incubated for 4 h at 37˚C. The absorbance to the manufacturer's protocol. Genomic DNA (250 ng) of was measured at a wavelength of 450 nm using a plate reader. each sample was bisulfite converted using EpiTect Bisulfite kit Each experiment was performed in triplicate. (cat. no. 59104; Qiagen, Inc.) according to the manufacturer's protocol. A 360 bp segment (nucleotides ‑977 to ‑617, tran‑ Western blot analysis. Total protein was extracted from frozen scriptional start site, +1) from bisulfate‑modified DNA was samples and cell lines using RIPA lysis buffer (Beyotime amplified using MSP DNA polymerase (TIANGEN Biotech Institute of Biotechnology). The protein concentration was Co., Ltd.) with the following primer sequences: Forward, estimated using a BCA assay and 20 µg protein/lane was sepa‑ 5'‑TGA TTA GAG TAG GGA TGG AAA G‑3' and reverse, 5'‑TAC rated via 10% SDS‑PAGE, and then transferred onto PVDF AAC CAA CAT CCC TAA AAA ‑3'. The thermocycling condi‑ membranes (MilliporeSigma). The membranes were blocked tions were as follows: 1 cycle at 95˚C for 10 min, followed by with 5% skimmed milk suspended in TBST at room tempera‑ amplification for 40 cycles at 95˚C for 30 sec, 60˚C for 30 sec ture for 2 h.
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